Relationship between NK Cells and Insulin Resistance in Adipose Tissue

As a consequence of sustained over nutrition, obesity has become epidemic in many countries worldwide. The prevalence rates are continuing to increase, most rapidly in developing countries. Obesity predisposes individuals to an increased risk of developing several diseases, including atherosclerosis, diabetes, non-alcoholic fatty liver disease and some certain cancers. Obesity, in particular visceral obesity, which is accumulation of adipose tissue inside the abdominal cavity, is associated with resistance to the effects of insulin [IR (insulin resistance)], often leading to the development of T2DM (Type 2 diabetes mellitus). In addition to these associations between obesity and disease, research in the past few years has identified important pathways that link metabolism with the immune system and vice versa. Many of these interactions between the metabolic and immune systems seem to be orchestrated by a complex network of soluble mediators derived from immune cells and adipocytes [1,2]. Obesity induced inflammation is the basis for the development of insulin resistance and type 2 diabetes. The most common underlying cause is central obesity, although insulin resistance is also possible in normal-weight individuals. Excess abdominal adipose tissue has been shown to release increased amounts of free fatty acids, tumor necrosis factor α (TNFα), adiponectin, leptin, IL-6 and some other adipokines, which affect insulin signalling [3]. The inflammatory response is mediated by immune cells in adipose tissue, macrophages infiltrate adipose tissue during obesity and contribute to insulin resistance [4]. In recent years it has been discovered that tissue-resident NK cells are key regulators of macrophage polarization and insulin resistance in response to obesity-induced adipocyte stress [5]. Visceral adipose tissue is more closely associated with insulin resistance than subcutaneous adipose tissue, according to the report [6]. NK cells, acting as an important immune cell, may be a cause of the different relationship between the two depot adipose tissue (visceral adipose tissue, VAT and subcutaneous adipose tissue, SAT) and insulin resistance.